| Project/Area Number |
25461158
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kobe University |
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Principal Investigator |
Tachihara Motoko 神戸大学, 医学(系)研究科(研究院), 助教 (40448626)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIMURA YOSHIHIRO 神戸大学, 医学部附属病院, 教授 (20291453)
KOBAYASHI KAZUYUKI 神戸大学, 大学院医学研究科, 講師 (50403275)
TAMURA DAISUKE 神戸大学, 医学部附属病院, 特定助教 (80646597)
NAGANO TATSUYA 神戸大学, 大学院医学研究科, 特命助教 (80624684)
小谷 義一 神戸大学, 医学(系)研究科(研究院), 講師 (90403287)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | アムルビシン / 薬剤耐性 / アンフィレグリン / 国際情報交換 |
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| Outline of Final Research Achievements |
Amrubicin (AMR) has shown promising activity for lung cancer. However, little is known about the mechanism of resistance for this agent.
Transcriptome analysis of amrubicinol (AMR-OH)-resistant lung cancer cell lines (H520/R, and DMS53/R) showed that amphiregulin (AREG) was most highly up-regulated gene in both of the AMR-OH-resistant cells compared to H520 and DMS53. AREG concentration in cultured medium of DMS53/R was higher compared to DMS53 after 72h culture with AMR-OH. A conditioned medium from DMS53/R decreased sensitivity to AMR-OH in DMS53. On the other hand, DMS53/R transfected with siRNA directed against AREG recovered sensitivity to AMR-OH. Additional administration of cetuximab (CET) on AMR-OH also recovered sensitivity to AMR-OH in DMS53/R. AMR/CET treatment showed higher antitumor activity in DMS53/R-bearing mice than AMR treatment.
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